Difference between revisions of "Polyneuritis Equi"

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Also know as: '''''Neuritis of the cauda equina — Cauda equina syndrome — Cauda equina neuritis'''''
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 +
Also know as: '''''Neuritis of the Cauda Equina — Cauda Equina Syndrome — Cauda Equina Neuritis — PNE'''''
  
 
==Introduction==
 
==Introduction==
 
Polyneuritis equi is uncommon and caused by a '''progressive immune-mediated lymphocytic infiltration and demyelination''' of the sacrococcygeal and lumbosacral nerve roots of the '''cauda equina'''. Nerves outside the cauda equina, such as the '''cranial nerves''', may also be affected.
 
Polyneuritis equi is uncommon and caused by a '''progressive immune-mediated lymphocytic infiltration and demyelination''' of the sacrococcygeal and lumbosacral nerve roots of the '''cauda equina'''. Nerves outside the cauda equina, such as the '''cranial nerves''', may also be affected.
  
The aetiology of the disease is unknown, but evidence suggests that it is an allergic-mediated polyneuropathy similar to '''Guillain-Barré syndrome in humans''' and experimental allergic neuritis (EAN) of laboratory rodents. Infection with Equine Herpesvirus-1 and Campylobacter have been proposed, but there has been no confirmation.
+
The aetiology of the disease is unknown, but evidence suggests that it is an allergic-mediated polyneuropathy similar to '''Guillain-Barré syndrome in humans''' and experimental allergic neuritis (EAN) of laboratory rodents. Infection with [[Equine Herpesvirus 1|Equine Herpesvirus-1]] and ''[[Campylobacter species - Overview|Campylobacter]]'' have been proposed, but there has been no confirmation.
  
It is seen in '''adult horses of all breeds in North American and Europe'''.
+
It is seen in '''adult horses of all breeds in North America and Europe'''.
  
==Clinical signs==
+
==Clinical Signs==
 
Typically, there is a '''slow progressive paralysis''' of the tail, rectum, anus and bladder and hindlimb weakness and ataxia.
 
Typically, there is a '''slow progressive paralysis''' of the tail, rectum, anus and bladder and hindlimb weakness and ataxia.
  
 
There will be '''urine scalding''' of the hindlimbs, hyperaesthesia and muscle fasciculations over the hindquarters.
 
There will be '''urine scalding''' of the hindlimbs, hyperaesthesia and muscle fasciculations over the hindquarters.
  
'''Muscle atrophy''' is variable present.
+
'''Muscle atrophy''' is variably present.
  
'''Cranial nerve involvement''', particularly CN V, VII and VIII, may also be present and is usually asymmetric. This will present as paralysis of the facial muscles, head tilt, nystagmus, tongue paralysis and difficulty swallowing.
+
'''[[Cranial Nerves - Anatomy & Physiology|Cranial nerve]] involvement''', particularly CN V, VII and VIII, may also be present and is usually asymmetric. This will present as paralysis of the facial muscles, head tilt, nystagmus, tongue paralysis and difficulty swallowing.
  
 
==Diagnosis==
 
==Diagnosis==
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The diagnosis is one of '''exclusion''', supported by the clinical signs and history.
 
The diagnosis is one of '''exclusion''', supported by the clinical signs and history.
  
An ELISA can be performed to detect '''antibodies against P2-myelin protein''', but the test is not available commercially and is not specific for the disease.
+
An [[ELISA testing|ELISA]] can be performed to detect '''antibodies against P2-myelin protein''', but the test is not available commercially and is not specific for the disease.
  
 
On routine '''haematology''': evidence of chronic inflammation is usually detected.
 
On routine '''haematology''': evidence of chronic inflammation is usually detected.
  
Analysis of the '''CSF''' reveals: xanthochromia and a mildly increased protein and cell count.
+
Analysis of the [[Cerebral Spinal Fluid - Anatomy & Physiology|'''CSF''']] reveals: xanthochromia and a mildly increased protein and cell count.
  
 
'''Differential diagnoses''' that should be ruled out before a diagnosis of PNE is considered include:
 
'''Differential diagnoses''' that should be ruled out before a diagnosis of PNE is considered include:
 
+
:[[Equine Herpesvirus 1|Equine herpesvirus-1]] myeloencephalopathy
:Equine herpesvirus-1 myeloencephalopathy
 
 
:Sacral/coccygeal trauma
 
:Sacral/coccygeal trauma
:Equine motor neuron disease
+
:[[Equine Motor Neuron Disease|Equine motor neuron disease]]
:Abberant parasite migration (e.g. ''Strongylus spp.'')
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:Abberant parasite migration (e.g. [[:Category:Strongyloidea|''Strongylus spp.'']])
:In endemic areas, such as the USA ''Sarcocystis neurona'' myelitis (equine protozoal myelitis)
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:In endemic areas, such as the USA ''[[Sarcocystis|Sarcocystis neurona]]'' myelitis ([[Equine Protozoal Myeloencephalitis|equine protozoal myelitis]])
:Rabies and ''Rhodococcus equi'' myeloencepahlitis should also be considered.
+
:[[Rabies]] and ''[[Rhodococcus equi]]'' myeloencephalitis should also be considered.
  
The definitive diagnosis is made on '''post-mortem examination'''.
+
The definitive diagnosis is made on '''post-mortem examination'''. Extradural and intradural nerve roots of the cauda equina are grossly thickened and are infiltrated with inflammatory cells. Demyelination and axonal degeneration are present. Similar changes in the cranial nerves may be observed.
 
 
Extradural and intradural nerve roots of the cauda equina are grossly thickened and are infiltrated with inflammatory cells. Demyelination and axonal degeneration are present. Similar changes in the cranial nerves may be observed.
 
  
 
==Treatment==
 
==Treatment==
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Furr, M. (2008) '''Equine Neurology''' ''John Wiley and Sons''
 
Furr, M. (2008) '''Equine Neurology''' ''John Wiley and Sons''
  
[[Category:To Do - Helen]]
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{{review}}
[[Category:To Do - Review]]
 
 
 
 
 
Cauda Equina Traction - in small animals
 
:Tail pull injury
 
:Esp. cats after RTA
 
:Lesion via longitudinal traction
 
:Sacrocaudal dislocation/fracture
 
:Limp tail
 
:Incontinence
 
:Hindlimb Paresis
 
:Diagnosis on Clinical signs and history
 
:+/- Radiographs to show dislocation/fracture
 
:Prognosis difficult to predict
 
:Poor prognosis if tail limp & no anal tone
 
:Supportive treatment
 
:Persist for >3 months if possible
 
  
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==Webinars==
 +
<rss max="10" highlight="none">https://www.thewebinarvet.com/neurology/webinars/feed</rss>
  
 +
[[Category:Neurological Diseases - Horse]]
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[[Category:Expert Review - Horse]]
 
[[Category:Central Nervous System - Idiopathic Pathology]]
 
[[Category:Central Nervous System - Idiopathic Pathology]]
 
[[Category:Peripheral Nervous System - Pathology]]
 
[[Category:Peripheral Nervous System - Pathology]]

Latest revision as of 16:47, 6 January 2023

Also know as: Neuritis of the Cauda Equina — Cauda Equina Syndrome — Cauda Equina Neuritis — PNE

Introduction

Polyneuritis equi is uncommon and caused by a progressive immune-mediated lymphocytic infiltration and demyelination of the sacrococcygeal and lumbosacral nerve roots of the cauda equina. Nerves outside the cauda equina, such as the cranial nerves, may also be affected.

The aetiology of the disease is unknown, but evidence suggests that it is an allergic-mediated polyneuropathy similar to Guillain-Barré syndrome in humans and experimental allergic neuritis (EAN) of laboratory rodents. Infection with Equine Herpesvirus-1 and Campylobacter have been proposed, but there has been no confirmation.

It is seen in adult horses of all breeds in North America and Europe.

Clinical Signs

Typically, there is a slow progressive paralysis of the tail, rectum, anus and bladder and hindlimb weakness and ataxia.

There will be urine scalding of the hindlimbs, hyperaesthesia and muscle fasciculations over the hindquarters.

Muscle atrophy is variably present.

Cranial nerve involvement, particularly CN V, VII and VIII, may also be present and is usually asymmetric. This will present as paralysis of the facial muscles, head tilt, nystagmus, tongue paralysis and difficulty swallowing.

Diagnosis

Currently there are no specific antemortem tests to detect the disease in horses.

The diagnosis is one of exclusion, supported by the clinical signs and history.

An ELISA can be performed to detect antibodies against P2-myelin protein, but the test is not available commercially and is not specific for the disease.

On routine haematology: evidence of chronic inflammation is usually detected.

Analysis of the CSF reveals: xanthochromia and a mildly increased protein and cell count.

Differential diagnoses that should be ruled out before a diagnosis of PNE is considered include:

Equine herpesvirus-1 myeloencephalopathy
Sacral/coccygeal trauma
Equine motor neuron disease
Abberant parasite migration (e.g. Strongylus spp.)
In endemic areas, such as the USA Sarcocystis neurona myelitis (equine protozoal myelitis)
Rabies and Rhodococcus equi myeloencephalitis should also be considered.

The definitive diagnosis is made on post-mortem examination. Extradural and intradural nerve roots of the cauda equina are grossly thickened and are infiltrated with inflammatory cells. Demyelination and axonal degeneration are present. Similar changes in the cranial nerves may be observed.

Treatment

Treatment is palliative, including managmenent of urinary and faecal incontinence, managing cystitis and minimising urine scalding.

Horses with dysphagia may need tube feeding.

Treatment with corticosteroids has provided some palliative benefits but the effect is short-lived.

The condition is slowly progressive, but the prognosis is generally poor.


Polyneuritis Equi Learning Resources
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Flashcards
Test your knowledge using flashcard type questions
Equine Orthopaedics and Rheumatology Q&A 06


References

DeLahunta, A. (2008) Veterinary neuroanatomy Elsevier Health Sciences

Merck and Co (2008) Merck Veterinary Manual Merial

Taylor, F. (2009) Diagnostic techniques in equine medicine Saunders

Furr, M. (2008) Equine Neurology John Wiley and Sons


Webinars

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